This study examines the mechanisms that account for abnormalities of platelet function in patients with bleeding disorders. During the primary arrest of bleeding, platelets adhere to components of the subendothelium and subsequently release adenosine diphosphate (ADP) by a mechanism known as the release reaction. This released ADP then results in platelet aggregation and the latter is responsible for the arrest of bleeding after injury to a blood vessel. Abnormalities in hemostasis may result from impaired adhesion of platelets to components of the subendothelium, from defects in the release reaction or from impairment of ADP-induced platelet aggregation. The mechanism that may account for these defects are the subjects of study in the present investigation.